Drug resistance is the phenomenon whereby widespread use of an antibacterial drug is followed by the emergence of strains of bacteria capable of resisting the drug.

In 1940, the New York Times hailed the arrival of

A new wonder-working chemical named sulfathiazole, the latest "relative" of the sulfanilimide group of "magic bullets," which promises to become the greatest weapon against a host of deadly bacterial infections for which no effective measures existed until now.[1]

Sulfa drugs followed the prior discovery of the first antibiotic, penicillin, and streptomycin, another antibiotic, was discovered not long after sulfathiazole. The revolutionary impact of these drugs cannot be overstated. Previously there had been an obsession with the threat of germs[2] because infections, once contracted, were often fatal. With antibiotics, for the first time in human history, serious bacterial diseases could be cured promptly and effectively. The phrases "wonder drug" and "miracle drug" were widely used.

But pencillin-resistant microbes started to appear in 1947, just four years after it entered widespread use.[3] By 1952 the Times was reporting that "more bacteria [are] developing more resistance to 'wonder drugs.'"[4]

Bacteriologists soon found that E. coli grown in media containing streptomycin not only produced strains capable of resisting streptomycin, they actually in some cases developed strains that thrived on it and required it for growth.

In the last half of the twentieth century, a situation developed which was often described as an "arms race" between doctors and bacteria. Bacteria kept developing resistance to drugs, but researchers and drug companies kept ahead of them by developing new drugs. Drug company representatives combed the world collecting soil samples and biological specimens, looking for useful antibiotics in nature, while chemists tried to synthesize new antibiotics in the laboratory. The 1960s saw the emergence of a number of synthetic penicillin-like drugs, such as ampicillin, amoxicillin, and cloxacillin. But by the 1990s the development and discovery of entirely new classes of antibiotics appeared to have reached an end; scientists only managed to make improvements within existing classes of drugs.[5] There is widespread concern that the bugs are catching up. The generation now approaching retirement may be the only human generation in history to live its entire life free from the mortal dread of bacterial infection.

Gonorrhea, for example, was once regarded as easily curable with penicillin. In the 1980s, penicillin-resistant strains developed, but gonorrhea was still not considered dangerous; it was still curable, it just required newer antibiotics. The main public health concern was that effective treatment had now become more expensive. In 2007, it emerged as a "superbug" for which a single treatment option is still effective. Thus, although standard references still say "In most cases, the disease can be cured by adequate treatment with a fluoroquinolone or cephalosporin antibiotic,"[6] the Center for Disease Control now finds that resistance to the fluoroquinolones is so widespread that it no longer recommends them as a treatment for gonorrhea in the United States.[7].

There is controversy over the best policies to keep drug-resistant strains in check. In the 1940s the medical profession began lobbying to make antibiotics available only through prescription to prevent overuse, and educating doctors to be prudent in prescribing them. However, antibiotics are widely added to livestock feed to prevent infection and promote growth, and critics charge that the practice has encouraged the emergence of resistant strains, a charge which the agriculture industry and the USDA deny.

The mechanism by which drug resistance emerges was studied by Luria and Delbrück in 1943 and by Lederburg and Lederburg in 1952. Further work established that streptomycin resistance emerges as the result of point mutations, at a rate of about one per billion cells, while isoniazid resistance has a mutation rate of one per million.

Drug resistance also arises in viruses. For example, the anti-flu drug Oseltamivir (Tamiflu) was only introduced in the year 2000, and did not receive widespread use until 2004; yet in 2007, type B influenza infections resistant to the drug were observed in Japan.[8]

Drug resistance is also used in many molecular biology techniques. A plasmid containing a gene of interest and a gene for antibiotic resistance is transformed into a strain of bacteria (usually E.Coli) via chemical or electrical means. The bacteria is then plated onto media containing the antibiotic corresponding to the gene of antibiotic resistance. Only bacteria that have taken up the plasmid containing the antibiotic resistance gene can grow on the media. The plasmid containing the gene of interest can then be purified via alkaline lysis.

Drug resistance and evolution

The development of antibiotic resistance is often held up by evolutionists as proof of evolution occurring, however the appearance of resistant organisms is often proceeded by the uptake of transposable epigenetic elements (TEEs) called plasmids. These TEEs are found in related organisms and the resistance to any given class of antibiotics is merely transferred from one strain to another to make a new hybrid strain. [9]